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MCG > METABOLISM SYLLABUS 1: Intro to Metabolism & to Metabolic Regulation by Insulin & Glucagon > Flashcards

METABOLISM SYLLABUS 1: Intro to Metabolism & to Metabolic Regulation by Insulin & Glucagon Flashcards

1
Q

metabolism?

A

sequence of enzyme-catalyzed reactions that brings about the transformation of substrate to product

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2
Q

major purposes of metabolism?

A

1) obtain & trap chemical energy from substrates
2) build precursors to macromolecules from substrates
3) assemble precursors into macromolecules like DNA, glycogen, fat
4) degrade macromolecules into simpler molecules (like glycogen to glucose)

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3
Q

catabolism vs. anabolism?

A

catabolism: oxidative breakdown of large macromolecules into smaller, simpler compounds. accompanied by release of free energy, trapping it as ATP - e.g. glucose -> pyruvate

anabolism: enzymatic synthesis of large macromolecules from smaller, simpler precursors. requires energy input - e.g. pyruvate -> glucose

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4
Q

what are amphibolic pathways?

A

pathways w/ both cataboilc and anabolic components - so can both breakdown and synthesize

e.g. TCA cycle

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5
Q

what are the major differences in catabolism and anabolism? why?

A

1) ENZYMES

2) ENERGETICS: ATP made in catabolism, used in anabolism

3) COFACTORS: NAD+->NADH in catabolism and NADPH -> NADP+in anabolism

4) CELLULAR LOCALIZATION: fatty acid oxidation in th emito, fatty acid synthesis in the cyto

identical pathways would prevent regulation, lead to futile cycling and energy waste

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6
Q

what regulates metabolism?

A

1) availability and concetration of substrates & cofactors
2) availability and need for energy/ATP
3) regulatory enzymes
4) enzyme characteristics
5) genetic control of amt of enzyme in cell
6) hormonal regulation

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7
Q

what is end product feedback inhibition?

A

principle that anabolic reations are often inhibited by products of that very anabolic reaction

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8
Q

constituitive vs. adaptive enzymes?

A

constituitive: enzymes that’re always present in constant or near-constant amount; are the more important enzymes

adaptive: enzymes that can increase or diecrease under certain metabolic conditions, in reaction to a substrate, toxin, or drug which changes their amount in response to a signal

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9
Q

hormones?

A

chemical messenger produced in a tissue which will modify a specific metabolic reaction in aonther tissue

often acts on regulatory enzymes or activates or represses gene expression

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10
Q

what methods can determine the rate limiting step in a biochemical pathway?

A

1) assays on relative activites
2) comparisons of the equilibrium constant to the mass action ratio

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11
Q

which enzyme in a pathway is the rate limiting enzyme?

A

enzyme with the lowest relative activity and enzymes with big discrepancy between their Keq and mass action ratio

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12
Q

what are the rate limiting enzymes of glycolysis?

A

hexokinase, phosphofructokinase, and pyruvate kinase

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13
Q

what is the effect of an inhibitor on a rate-limiting vs. non-rate-limiting enzyme?

A

an inhibitor of a rate-limiting enzyme inhibits the overall pathway

an inhibitor of a non-rate-limiting enzyme inhibits the enzyme but likely not the overall pathway

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14
Q

what enzymes are most likely to be regulated?

A

relatively low active enzymes and enzymes that fail to maintain equilibrium are likely to be regulated

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15
Q

what is the RBC’s only form of energy?

A

glucose. they do not have mitochondria!

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16
Q

what organi is the major controller of our metabolism?

A

liver

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17
Q

what processes during glycolysis cause the release of ATP?

A

susbtrate level phosphorylation or oxidative phosphorylation

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18
Q

what kind of energy does ATP hydrolysis yield?

A

ATP -> ADP + Pihas a deltaG of 7-8 Kcal/mol

ATP is a high energy compound, and yields a middle-amount of energy compared to other compounds

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19
Q

what happens when ATP is hydrolyzed to ADP?

what happens when ATP is hydrolyzed to AMP?

A

ATP -> ADP + Pidissipates 1 high energy bond

ATP -> AMP + PiPidissipates 2 high energy bonds

PiPi, pyrophosphate, is rapidly hydrolyzed to 2 molecules of Piby pyrophosphatase

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20
Q

what is the structure of NAD+ vs NADH

A

NAD+ is oxidized, NADH is reduced

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21
Q

what is the difference between FAD and FADH2?

A

FAD is oxidized, FADH2 is reduced

22
Q

what hormones regulate glucose/fatty acid metabolism?

A

insuiln, glucagon, epinephrine (epi)

insulin + epi regulate glucose & fatty acid metabolism in mayn tissues

glucagon acts primarily on the liver & adipose tissue

23
Q

where is epi produced? when?

A

in adrenal glands

in response to stress

produced from phenylalanine + tysoine by catacholamine synthesis pathway

24
Q

where are insulin and glucagon produced? when?

A

beta (insulin) and alpha (glucagon) cells of the pancrease

in response to glucose levels:

INSULIN in response to HIGH glucose (high carb diet)

GLUCAGON in response to LOW glucose (starvation)

25
Q

primary function of insulin?

A

promote use of glucose

26
Q

primary function of glucagon?

A

promote production of glucose by the liver

27
Q

what causes type 1 diabetes?

A

destruction of the B cells of teh pacnreas largely via autoimmune attack on these cells leads to lack of insulin production

28
Q

what causes type 2 diabetes?

A

insulin is produced but its effectiveness in enhancing utilization of glucose is decreased, which means increased resistance to actions of insulin

29
Q

what do obesity + lack of exercise lead to

A

type 2 diabetes

30
Q

what metabolic problems does diabetes cause

A

build up of high levels of glucose, esp. in the blood, lead to:

1) impaired energy production from glucose
2) fat metabolism’s elevated to provide energy, but much fat is oxidized to acidic ketone bodies -> ketosis
3) high circulating glucose levesl react non-enzymatically w/ prteins/enzymes, glycosylate them, form modified proteins w/ altered funtions
4) glucose can be reduced by aldose reducatse to sorbitol which increaes osmotic pressure

31
Q

what is assay for measuring long-term blood glucose levels?

A

hemoglobin A1c level - measures that hemoglobin reacts w/ high glucose to form hemoglobin A1c, a glycosylated hemoglobin

high levels of A1c (> 7 mg%) indicate poor glucose control

32
Q

what are glucagons functions

A

1) promotes glucose production in the liver by gluconeogenesis and stimulation of glycogen breakdown
2) increases fatty acid release from triglycerides stored in adipose tissue

33
Q

glycogen is?

A

polymer made of many glucose residues

functions as storage form of glucose

34
Q

how does glucagon exert its effects?

A

1) by stimulating the activites of critical enzymes involved in synthesis of glucose & breakdown of glycogen and fat
2) by transcriptionally activating the genes for these critical enzymes

35
Q

what are insulin’s main actions?

A

promotes utilization of glucose by

1) stimulating glycolysis
2) stimulating glucose uptake in some tissues like muscle & adipose tissue
3) stimulating glycogen formation
4) stimulating fatty acids synthesis from glucose
5) stimulating protein synthesis

36
Q

how does insulin exert its effects?

A

1) by increasing critical enzyme activities
2) by increasing synthesis of these enzymes

37
Q

how do insulin/glucagon work in relation to each other? what pathways does each stimulate/inhibit?

A

they work in opposite actions - so glucagon does the opposite of everything here

**insulin stimulates: **glucose-utilizing pathways: glycolysis, glycogen synthesis, fatty acid synthesis

insulin inhibits: gluconeogenesis, glycogen breakdown, fat breakdown

38
Q

how does insulin exert its effects?

A

via the insulin receptor on the plasma membrane of all tissues

insulin receptor has 2 alpha + 2 beta subunits. insulin binds alpha subunits, which span membrane, causing tyrosine kinase activity/dimerization of beta subunits, yielding phoshphotyrosine residues

the phosphotyrosine residues of beta subunit phosphorylate proteins IRS-1 and IRS-2

phosphorylated IRS-1 and IRS-2 phosphoryate & activate PI# kinase, which activates AKT

pAKT activates phosphatases, PKC, mTOR, which carry out insulin’s actions

take away: insulin binding stimulates activity of protein phosphatases which carry out downstream actions of insulin

39
Q

what is the structure of glucagon and epi receptors?

A

glucagon’s are in liver, fat tissues; epi’s are widely present

both are GPCRs with 7 TM spanning loops

alpha subunit binds GDP in inactive state

activated lgucagon or epi receptor catalyzes exchange of GDP with GTP; follwed by dissociation of beta-gamma subunits to form activate a-GTP G protein

this activates adenylate cyclase to produce cyclic AMP

cAMP activates PKA by binding to and dissociating regulatory subunits of PKA

this frees activte catalytic subunits of PKA

PKA promotes phoshporylation of many enzymes important in metabolism of glucose and fat - these phoshporylations may activate or inhbit the enzyme or txn factor

40
Q

what is the difference in phosphorylation btwn glucagon/epi and insulin?

A

glucagon and epi: promote phosphrylation of enzymes by activating cAMP-dependent PKA

insulin: promotes dephosphorylation of enzymes by activating phosphatases eg protein phosphatase 2A

41
Q

how is the glucagon/epi signal turned off?

A

alpha-GTP subunit has a GTPase activity; with time, GTP is hydrolyzed to form alpha-GDP subunit

this reassociates w/ the Beta-gamma subunits, reestablishes the inactive GDP-alpha-beta-gamma G protein

eventually, glucagon and epi dissociate from the receptor

also, cAMP is hydrolyzed by phosphodiesterase to AMP; so cAMP-PKA signal is turned off

42
Q

what does insulin do to phoshpodiesterase?

A

increases phosphodiesterase activity

phosphodiesterase hydrolyzes cAMP to AMP, turning off the cAMP-PKA signal

this is a way then that insulin counters the actions of glucagon and epi

43
Q

what is difference in glucagon/insulin re:

  • where each is made
  • what it activates
  • its target
  • when it is released
A
44
Q

why do glucose carriers exist?

A

glucose is highly polar structure - does not get into cells well, considering all of its OH groups

thus need glucose transporters/carriers to carry glucose from our diet into our cells

45
Q

how would you prove glucose uptake occurs by a carrier?

A

1) kinetics: plot energy vs. velocity curve, see that will eventually saturate the carrier
2) **specificity: **apply inhibitors and show that carriers are specific re: what they uptake

46
Q

what are the functions of GLUT1 and GLUT3 carriers?

where do they work?

when are they saturated?

A

work in most all tissue - liver, RBC, brain, pancreas, most cells

do passive carrier-mediate glucose transport

have a low Km/high affinity for glucose (1mM) so **catalyze basal glucose uptake **

they thus are **almost always saturated at normal glucose levels **since normal glucose is 4-8 mM

47
Q

what is GLUT2 carrier function?

where is it present?

what is its function?

A

**high kM, low affinity **for glucose (15-20 mM kM)

present in liver and pancreas

senses** high glucose **levels - for pancreas to produce insulin, and liver to utilize high glucose

48
Q

does insulin effect rate of glucose uptake by GLUT 1, 2, 3?

A

no

49
Q

where is GLUT4?

function?

A

muscle, fat cells

is the insulin responsive glucose transporter

insulin elevates number of GLUT4 carriers on plasma membrane of muscle and fat cells so glucose uptake is elevated

does this by translocating GLUT4 from Golgi to PM

this is a way to increase glucose uptake in muscle and fat cells

fat converts glucose -> fat, triglycerides

muscle converts glucose -> glucose, stored as glycogen

50
Q

GLUT5 function, location?

A

GI tract and kidney

catalyzes active transport of glucoses

moves molecules against concentration gradient; linked w/ Na+ transport

MCG (77 decks)

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